ArticleMolecular biology of the cell1999
The formation of an insulin-responsive vesicular cargo compartment is an early event in 3T3-L1 adipocyte differentiation.
Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 70 citations in OpenAlex.
- EFR3 and phosphatidylinositol 4-kinase IIIα regulate insulin-stimulated glucose transport and GLUT4 dispersal in 3T3-L1 adipocytes.Bioscience reports · 2022Article
- Article
- Microtubules in insulin action: what's on the tube?Trends in endocrinology and metabolism: TEM · 2021Review
- Insulin-responsive amino peptidase follows the Glut4 pathway but is dispensable for the formation and translocation of insulin-responsive vesicles.Molecular biology of the cell · 2019Article
- Characterization of VAMP isoforms in 3T3-L1 adipocytes: implications for GLUT4 trafficking.Molecular biology of the cell · 2015Article
- The Structural Basis of Action of Vanadyl (VOCoordination chemistry reviews · 2014Article
- Rab5 activity regulates GLUT4 sorting into insulin-responsive and non-insulin-responsive endosomal compartments: a potential mechanism for development of insulin resistance.Endocrinology · 2014Article
- Insulin responsiveness of glucose transporter 4 in 3T3-L1 cells depends on the presence of sortilin.Molecular biology of the cell · 2013Article
- Sorting of GLUT4 into its insulin-sensitive store requires the Sec1/Munc18 protein mVps45.Molecular biology of the cell · 2013Article
- Single point mutations result in the miss-sorting of Glut4 to a novel membrane compartment associated with stress granule proteins.PloS one · 2013Article
- Regulation of GLUT4 and Insulin-Dependent Glucose Flux.ISRN molecular biology · 2012Review
- Transdifferentiation of MALME-3M and MCF-7 Cells toward Adipocyte-like Cells is Dependent on Clathrin-mediated Endocytosis.SpringerPlus · 2012Article
- Identification of three distinct functional sites of insulin-mediated GLUT4 trafficking in adipocytes using quantitative single molecule imaging.Molecular biology of the cell · 2010Article
- Proteomic analysis of GLUT4 storage vesicles reveals LRP1 to be an important vesicle component and target of insulin signaling.The Journal of biological chemistry · 2010Article
- The C-terminus of GLUT4 targets the transporter to the perinuclear compartment but not to the insulin-responsive vesicles.The Biochemical journal · 2009Article
- Self-assembly of Glut4 storage vesicles during differentiation of 3T3-L1 adipocytes.The Journal of biological chemistry · 2008Article
- Molecular mechanisms controlling GLUT4 intracellular retention.Molecular biology of the cell · 2008Article
- Inhibition of GLUT4 translocation by Tbc1d1, a Rab GTPase-activating protein abundant in skeletal muscle, is partially relieved by AMP-activated protein kinase activation.The Journal of biological chemistry · 2008Article
- The GLUT4 code.Molecular endocrinology (Baltimore, Md.) · 2008Review
- p115 Interacts with the GLUT4 vesicle protein, IRAP, and plays a critical role in insulin-stimulated GLUT4 translocation.Molecular biology of the cell · 2005Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Differentiating 3T3-L1 cells exhibit a dramatic increase in the rate of insulin-stimulated glucose transport during their conversion from proliferating fibroblasts to nonproliferating adipocytes. On day 3 of 3T3-L1 cell differentiation, basal glucose transport and cell surface transferrin binding are markedly diminished. This occurs concomitant with the formation of a distinct insulin-responsive vesicular pool of intracellular glucose transporter 1 (GLUT1) and transferrin receptors as assessed by sucrose velocity gradients. The intracellular distribution of the insulin-responsive aminopeptidase is first readily detectable on day 3, and its gradient profile and response to insulin at this time are identical to that of GLUT1. With further time of differentiation, GLUT4 is expressed and targeted to the same insulin-responsive vesicles as the other three proteins. Our data are consistent with the notion that a distinct insulin-sensitive vesicular cargo compartment forms early during fat call differentiation and its formation precedes GLUT4 expression. The development of this compartment may result from the differentiation-dependent inhibition of constitutive GLUT1 and transferrin receptor trafficking such that there is a large increase in, or the new formation of, a population of postendosomal, insulin-responsive vesicles.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.